Study Indicates
Pesticides May Effect Pre-pubescent Breast Development
(Beyond Pesticides, December 21, 2005) A recent study
led by Elizabeth Guillette and published in Environmental Health
Perspectives indicates that pesticides, such as those that effect
the endocrine system, may be having more of an effect on breast development
in young girls before age ten than previously thought.

The
study examined precocious puberty (early development of initial
breast and pubic hair development) in 50 healthy young girls ages eight
to ten with no signs of birth defects or tumors living in two agricultural
regions in the Yaqui Valley of Sonora, Mexico – one with little
to no pesticide exposure and one with pesticide exposure. The study
found a distinct difference between the populations. Research showed
a poorly defined relationship between the breast size and mammary gland
development of the population of young girls exposed to agricultural
pesticides and a robust positive relationship between breast size and
mammary size among the unexposed population.

Among the girls
exhibiting breast development and exposed to pesticides, palpable mammary
tissue development was lacking in 12 of the 27 pubescent girls. Comparitively,
non of the pubescent lesser-exposed girls exhibiting breast development
lacked palpable mammary tissue.

The authors hypothesize
“that an altered relationship between breast size, fat deposition,
and mammary tissue development could result from in utero and/or childhood
exposures to estrogenic or anti-androgenic chemicals as has been reported
in studies of laboratory rodents.”

The age at which
females exhibit breast development has been declining in some human
populations over the past fifty years. The reasons around which confound
scientists. The process and timing of puberty is made up of complex
interactions between neural and sex hormones. Many factors may influence
the process including genetic makeup, nutritional and lifestyle factors,
and possible cumulative exposure to environmental estrogens beginning
in the fetus and continuing until adulthood.

The authors were
careful to account for these factors in monitoring the studied populations
of the two regions. Lifestyle factors are essentially the same between
the populations. Prior dietary studies determine that the types of food
and amount served are similar in the two areas with continual exposure
through ingestion of pesticide residues on purchased foods. Both also
have limited exposure to plastics, makeup and treated wood furniture
that may off-gas. Prior cord blood studies in 1990 from infants born
in the agricultural towns two years prior to the birth of the girls
participating in the study indicated trans-placental transfer of high
levels of organochlorines such as Lindane and DDT metabolites.

The standard measure
to determine the staging of puberty and breast development, known as
the Tanner scale, primarily involves visual scaling. In this landmark
study, the authors analyzed morphometric data including breast size,
mammary gland development and fat deposition of breast tissue. Results
of the study indicated that using the additional variables shows distinct
differences between the populations while the method of visual staging
alone would show no difference. The data suggest that more in depth
studies are required in order to understand the environmental influences
on this increasing phenomenon.

The authors note
that, “The role of endocrine disrupting chemicals (EDCs) on the
puberty continuum has received limited attention but several reviews
suggest a need for more research. The exposure of laboratory animals
and wildlife to EDCs is known to alter the ratio of female to male hormones
that play a dominant role in sexual development. Exposure to some estrogen
mimics or anti-androgens can delay puberty in female rodents, whereas
experimental exposure to low doses of estrogenic Bisphenol A, found
in some plastics, speeds growth and puberty in rats.”